Genital infections caused by Chlamydia tracchomatis (CT) are among the most prevalent of sexually transmitted diseases. In addition, chlamydial pneumonitis in infants born to infected women is an important pediatric illness. We have developed a model for CT pneumonitis in C57BL/KsJ mice. In the proposed reserach our specific aims are to use the model: 1) to elucidate the pathogenesis, histopathology, immunopathology, and natural history of the disease; 2) to define the host immunologic mechanisms involved in response to and termination of the infection; 3) to assess to long-term pathologic sequellae of CT pneumonitis; 4) to investigate the role of prior immunity in the manifestations of host response and disease. We will determine the maximum sublethal dose of CT and the effect of anesthesia. We will define in detail the histopathology, immunopathology and time course of lesions in the nasopharynx, trachea, and lungs, and will define the components of the immune response involved in development of disease. We will look for fibrosis and increased collagen as long-term effects of CT pneumonitis, and finall we will compare the disease in mice from exposed and unexposed mothers. Mice will be examined using histo- and immunopathologic techniques and measurements of immune function. Our long term objective is the understanding of the mechanisms by which CT produces infant pneumonitis, which will have implications for other human CT diseases.